In order to better understand the mechanism of hypotension and bradycardia in newborn infants under halothane anesthesia, we studied the changes in the four determinants of cardiac output in newborn piglets given 0.5 and 1% end tidal halothane. Cardiac index (CI) was measured by thermodilution. Preload was estimated from the left ventricular diastolic dimension determined by echocardiography and from the left ventricular end-diastolic pressure. Total peripheral resistance index was calculated to assess afterload. Contractility was estimated from left ventricular peak dP/dT, and from left ventricular shortening fraction and mean rate of circumferential fiber shortening determined by echocardiography. All indices of contractility decreased to approximately 50% of baseline values during administration of 1% halothane, whereas heart rate (HR) was reduced to 74% of baseline. Preload and afterload did not change significantly. Mean arterial pressure (MAP) and CI decreased to 67% and 74% of control values, respectively. Smaller, proportional reductions in all variables occurred when 0.5% halothane was administered. Control values of MAP were the only measurements significantly related to piglet age. When five additional animals underwent atrial pacing at the control HR during 1% halothane anesthesia, MAP and CI decreased to 66 and 71% of control values, respectively. dP/dT/DP40, a dP/dT point measurement independent of preload and afterload changes, decreased to 49% of control during pacing. Therefore, the major effect of halothane in newborn piglets is its potent negative inotropic action, not peripheral vasodilation or bradycardia.